VALVULAR HEART DISEASE

VALVULAR HEART DISEASE Internal Medicine Didactics August 12, 2009 Steven R. B ruhl MD, MS

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Goals and Objectives • Discuss the common etiologies of valvular stenosis and regurgitation. • Recognize the signs and symptoms of severe valvular stenosis and regurgitation • Be able to quickly identify and treat acute mitral and aortic regurgitation • Identify patients who should be referred for surgical replacement of their valves

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Overview • Aortic Stenosis • Mitral Stenosis • Aortic Regurgitation – Acute and Chronic • Mitral Regurgitation – Acute and Chronic

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• Etiology • Pathophysiology • Physical Exam • Natural History • Testing • Treatment

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Aortic Stenosis

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Aortic Stenosis Overview: • Normal Aortic Valve Area: 3-4 cm2 • Symptoms: Occur when valve area is 1/4th of normal area. • Types: – Supravalvular – Subvalvular – Valvular

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Etiology of Aortic Stenosis • Congenital • Rheumatic • Degenerative/Calcific Patients under 70: >50% have a congenital cause Patients over 70: 50% due to degenerative

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Pathophysiology of Aortic Stenosis • A pressure gradient develops between the left ventricle and the aorta. (increased afterload) • LV function initially maintained by compensatory pressure hypertrophy • When compensatory mechanisms exhausted, LV function declines.

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Presentation of Aortic Stenosis – Syncope: (exertional) – Angina: (increased myocardial oxygen demand; demand/supply mismatch) – Dyspnea: on exertion due to heart failure (systolic and diastolic) – Sudden death

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Physical Findings in Aortic Stenosis • Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) • Heart sounds- soft and split second heart sound, S4 gallop due to LVH. • Systolic ejection murmur- cresendo- decrescendo character. This peaks later as the severity of the stenosis increases. – Loudness does NOT tell you anything about severity

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Natural History • Mild AS to Severe AS: – 8% in 10 years – 22% in 22 years– 38% in 25 years • The onset of symptoms is a poor prognostic indicator.

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Evaluation of AS • Echocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS. • Two measurements obtained are: a) Left ventricular size and function: LVH, Dilation, and EF b) Doppler derived gradient and valve area (AVA)

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Evaluation of AS Cardiac catheterization: Should only be done for a direct measurement if symptom severity and echo severity don’t match OR prior to replacement when replacement is planned.

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Management of AS • General- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. • Medical – limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS • Aortic Balloon Valvotomy- shows little benefit. • Surgical Replacement: Definitive treatment

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Echo Surveillance • Mild: Every 5 years • Moderate: Every 2 years • Severe: Every 6 months to 1 year

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Simplified Indications for Surgery in Aortic Stenosis • Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise) • Any patient with decreasing EF • Any patient undergoing CABG with moderate or severe AS

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Summary • Disease of aging • Look for the signs on physical exam • Echocardiogram to assess severity • Asymptomatic: Medical management and surveillance • Symptomatic: AoV replacement (even in elderly and CHF)

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Mitral Stenosis

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Mitral Stenosis Overview • Definition: Obstruction of LV inflow that prevents proper filling during diastole • Normal MV Area: 4-6 cm2• Transmitral gradients and symptoms begin at areas less than 2 cm2 • Rheumatic carditis is the predominant cause• Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.

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Etiology of Mitral Stenosis • Rheumatic heart disease: 77-99% of all cases • Infective endocarditis: 3.3% • Mitral annular calcification: 2.7%

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MS Pathophysiology • Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying) – worse with exercise, fever, tachycardia, and pregnancy • Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. • Right heart failure symptoms: due to Pulmonary venous HTN • Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

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Natural History of MS • Disease of plateaus: – Mild MS: 10 years after initial RHD insult – Moderate: 10 years later– Severe: 10 years later • Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism.

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Physical Exam Findings of MS • prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy • Signs of right-sided heart failure: in advanced disease • Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

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Heart Sounds in MS • Diastolic murmur: – Low-pitched diastolic rumble most prominent at the apex. – Heard best with the patient lying on the left side in held expiration – Intensity of the diastolic murmur does not correlate with the severity of the stenosis

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Heart Sounds in MS • Loud Opening S snap: heard at the apex when 1 leaflets are still mobile – Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips. – A shorter S2 to opening snap interval indicates more severe disease.

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Evaluation of MS • ECG: may show atrial fibrillation and LA enlargement • CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV • ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

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Management of MS Serial echocardiography: – Mild: 3-5 years– Moderate:1-2 years– Severe: yearly • Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression β-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling – Duiretics for fluid overload

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Management of MS • Identify patient early who might benefit from percutaneous mitral balloon valvotomy. • IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

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Simplified Indications for Mitral valve replacement • ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms • Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

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Aortic Regurgitation

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Aortic Regurgitation Overview • Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

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Etiology of Acute AR • Endocarditis • Aortic Dissection • Physical Findings: – Wide pulse pressure– Diastolic murmur– Florid pulmonary edema

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Treatment of Acute AR • True Surgical Emergency: • Positive inotrope: (eg, dopamine, dobutamine) • Vasodilators: (eg, nitroprusside) • Avoid beta-blockers • Do not even consider a balloon pump

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Etiology of Chronic AR • Bicuspid aortic valve • Rheumatic • Infective endocarditis

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Pathophysiology of AR • Combined pressure AND volume overload • Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

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Natural History of AR • Asymptomatic until 4th or 5th decade • Rate of Progression: 4-6% per year • Progressive Symptoms include: – Dyspnea: exertional, orthopnea, and paroxsymal nocturnal dyspnea – Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood pressure – Palpitations: due to increased force of contraction

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Physical Exam findings of AR • Wide pulse pressure: most sensitive • Hyperdynamic and displaced apical impulse • Auscultation- – Diastolic blowing murmur at the left sternal border– Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate – Systolic ejection murmur: due to increased flow across the aortic valve

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MRI of the Heart Revealing a Central, High-Velocity Jet Projecting into the Left Ventricular Cavity. The jet clearly strikes the anterior mitral-valve leaflet, causing distortion and premature closure during di astole.

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The Evaluation of AR • CXR: enlarged cardiac silhouette and aortic root enlargement • ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation) • Aortography: Used to confirm the severity of disease

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Management of AR • General: IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis. • Medical: Vasodilators (ACEI’s), Nifedipine improve stroke volume and reduce regurgitation only if pt symptomatic or HTN. • Serial Echocardiograms: to monitor progression. • Surgical Treatment: Definitive Tx

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Simplified Indications for Surgical Treatment of AR • ANY Symptoms at rest or exercise • Asymptomatic treatment if: – EF drops below 50% or LV becomes dilated

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Mitral Regurgitation

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Chronic Mitral Regurgitation Overview • Definition: Backflow of blood from the LV to the LA during systole • Mild (physiological) MR is seen in 80% of normal individuals.

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Acute MR • Endocarditis • Acute MI: • Malfunction or disruption of prosthetic valve

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Management of Acute MR • Myocardial infarction: Cardiac cath or thrombolytics • Most other cases of mitral regurgitation is afterload reduction: – Diuretics and nitrates – nitroprusside, even in the setting of a normal blood pressure.

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Management of Acute MR • Do not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.

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Treatment of Acute MR • Balloon Pump • Nitroprusside even if hypotensive • Emergent Surgery

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Etiologies of Chronic Mitral Regurgitation • Myxomatous degeneration (MVP) • Ischemic MR • Rheumatic heart disease • Infective Endocarditis

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Pathophysiology of MR • Pure Volume Overload • Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility – Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension. – Progressive left ventricular volume overload leads to dilation and progressive heart failure.

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Physical Exam findings in MR • Auscultation: soft S1 and a holosystolic murmur at the apex radiating to the axilla – S3 (CHF/LA overload)– In chronic MR, the intensity of the murmur does correlate with the severity. • Exertion Dyspnea: ( exercise intolerance)• Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

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The Natural History of MR • Compensatory phase: 10-15 years• Patients with asymptomatic severe MR have a 5%/year mortality rate • Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply • Mortality: From progressive dyspnea and heart failure

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Imaging studies in MR • ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR • CXR: LA enlargement, central pulmonary artery enlargement. • ECHO: Estimation of LA, LV size and function. Valve structure assessment – TEE if transthoracic echo is inconclusive

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Management of MR • Medications a) Vasodilator such as hydralazine b) Rate control for atrial fibrillation with β- blockers, CCB, digoxin c) Anticoagulation in atrial fibrillation and flutter d) Diuretics for fluid overload

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Management of MR • Serial Echocardiography: – Mild: 2-3 years – Moderate: 1-2 years – Severe: 6-12 months • IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

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Simplified Indications for MV Replacement in Severe MR • ANY Symptoms at rest or exercise with (repair if feasible) • Asymptomatic: – If EF <60%– If new onset atrial fibrillation

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THANK YOU

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